甲钴胺治疗糖尿病周围神经病的临床观察

糖尿病周围神经病是糖尿病常见的慢性并发症之一,其病变主要与长期高血糖及由此导致的代崩障碍、微循环异常和自身免疫紊乱有关。近年来应用甲钻胺治疗糖尿病周围神经病取得了较好的疗效。     

甲钴胺与前列腺素E1联合应用治疗周围神经病变疗效观察

观察前列腺素Ｅ１及甲钴胺联合应用对糖尿病性周围神经病变的疗效。方法：将２型糖尿病合并周围神经病变的病人分为两组,Ａ组给予ＰＧＥ１,Ｂ组合用甲钴胺。分别于疗程的第２、５、８周测定神经障碍的改善率并给予统计学处理。结论同时给予改善微循环的ＰＧＥ１和改善代谢的甲钴胺,可以显著提高显效率及总有效率,缩短疗程,增加闰人对治疗的耐受性。     

甲钴胺联合还原型谷胱甘肽治疗慢性酒精中毒性周围神经病疗效观察

目的观察甲钴胺联合还原型谷胱甘肽治疗慢性酒精中毒性周围神经病(CAPN)的临床效果。方法将本院神经内科就诊的52例CAPN患者随机分为治疗组和对照组,治疗组在常规治疗的基础上,给予甲钴胺500μg.d-1肌注,连用4周,同时静脉滴注还原型谷胱甘肽1200 mg.d-1,连续4周;对照组给予肌肉注射维生素,Vit B1100 mg.d-1、Vit B12500μg.d-1,共4周。比较两组治疗前后症状、体征及运动和感觉神经传导速度(MCV、SCV)的变化。结果与对照组比较,治疗组临床症状和体征明显改善,总有效率高于对照组(P<0.05),MCV和SCV有显著提高(P<0.05)。结论甲钴胺联合还原型谷胱甘肽能改善慢性酒精中毒性周围神经病患者的临床症状,提高神经传导速度(NCV),疗效确切。     

甲钴胺与前列腺素E_1联合应用治疗周围神经病变疗效观察

目的：观察前列腺素E_1（PGE_1）及甲钴胺联合应用对糖尿病性周围神经病变的疗效。方法：将2型糖尿病合并周围神经病变的病人分为两组,A组给予PGE_1（100ug,每日一次静滴,14天一疗程）,B组合用甲钴胺（500ug,隔日一次肌注,连续应用）。分别于疗程的第2、5、8周测定神经障碍的改善率并给予统计学处理。结果：①B组病人疗程末的总改善率分别为86．8％、92．5％和94．7％,明显高于A组的60．0％、77．5％和80．0％,除第5周外,均有统计学差异（P＜0．05）;②B组的显效率半数以上发生在第一疗程,并且各疗程的显效率较A组显著增高（P＜0．01）;结论：同时给予改善微循环的PGE_1和改善代谢的甲钴胺,可以显著提高显效率及总有效率,缩短疗程,增加病人对治疗的耐受性。     

甲钴胺联合神经节苷酯治疗慢性酒精中毒性周围神经病的临床分析

目的观察甲钴胺联合单唾液酸四己糖神经节苷酯(神经节苷酯)治疗慢性酒精中毒性周围神经病(CAPN)的临床疗效。方法选取48例确诊为慢性酒精中毒性周围神经病患者,随机分成治疗组和对照组,对照组给予甲钴胺及常规药物治疗,治疗组在此基础上加用神经节苷酯,治疗4周后的临床疗效采用症状体征和神经传导速度进行评价。结果治疗组总有效率为91.7%,对照组总有效率66.7%,治疗组总有效率比对照组高,差异有统计学意义(P0.05)。两组患者治疗后的正中神经和腓总神经的神经传导速度都有增加,治疗组比对照组增加更明显,差异有统计学意义(P0.05)。结论甲钴胺联合神经节苷脂治疗慢性酒精中毒性周围神经病变可显著改善患者的症状体征和神经传导速度,值得临床推广应用。     

甲钴胺治疗糖尿病周围神经病变临床观察

目的观察甲钴胺治疗糖尿病周围神经病变的疗效。方法将124例糖尿病周围神经病变患者随机分为2组,在严格控制血糖的基础上,治疗组64例,将甲钴胺500μg加入生理盐水250 ml中静滴,1次/d;对照组60例,除不用甲钴胺外其余治疗同治疗组。2组均以4周为一疗程,观察甲钴胺治疗糖尿病周围神经病变的疗效。结果治疗组总有效率为96.9%,对照组总有效率为53.3%。2组比较差异有显著性(P0.01)。在改善肌电图方面,治疗组明显优于对照组(P0.05)。结论甲钴胺是一种比较理想的治疗糖尿病周围神经病变的药物。     

甲钴胺治疗糖尿病周围神经病变疗效观察

目的 探讨甲钴胺治疗糖尿病周围神经病变的临床疗效.方法 将80例糖尿病病人随机分为对照组和治疗组,对照组40例进行基础治疗,即常规调整血糖,活血化瘀联合维生素B1、维生素B12,治疗组40例在基础治疗基础上再加用甲钴胺.结果 对照组总有效率75.0%,治疗组为87.5%,2组间比较差异有统计学意义(P＜0.05).结论...     

甲钴胺联合前列腺素E1治疗糖尿病周围神经病变临床观察

糖尿病周围神经病变是糖尿病最常见的慢性并发症之一.其病因主要与长期高血糖以及由此导致的代谢和微循环障碍有关.临床症状多以四肢持续性疼痛、麻木及感觉减退为主要表现[1].我院应用甲钴胺联合前列腺素E1治疗糖尿病周围神经病变效果满意现报告如下.     

甲钴胺治疗突发性耳聋的疗效观察

目的 观察甲钴胺治疗突发性耳聋的疗效.方法 突发性耳聋52例,随机分2组,每组26例.甲钴胺组采用甲钴胺治疗;对照组常规治疗.结果 2组病例治疗后耳聋症状均有改善,甲钴胺组与对照组相比较,有效率差异有统计学意义(P<0.05).结论 甲钴胺治疗突发性耳聋的疗效令人满意.     

The neurophysiologic investigation of small fiber neuropathies

We have applied our technique for the measurement of thermal thresholds to 25 patients referred with symptoms and signs of small fiber peripheral neuropathy in whom conventional electrophysiological indices were individually within the range of normal values for our laboratory. Vibration threshold determinations were also within normal range. Significant abnormalities of thermal thresholds were noted in all patients. The results indicate that the technique provides an accurate, easily performed and reproducible index of function in small A delta and C groups of nerve fibers.     

依帕司他与甲钴胺联合治疗糖尿病周围神经病变疗效观察

目的探讨依帕司他联合甲钴胺治疗糖尿病周围神经病变（DPN）的疗效。方法对96例DPN患者随机分为治疗组48例和对照组48例。在控制血糖血脂等治疗的基础上,治疗组采用依帕司他联合应用甲钴胺,对照组单用甲钴胺,8周后比较2组治疗前后症状、体征变化及神经传导速度（包括腓总神经和正中神经运动神经传导速度（MNCV）和感觉神经传导速度（SNCV）。结果治疗组总有效率87.50%,明显优于对照组64.58%（P〈0.01）;正中、腓总神经传导速度（MNCV和SNCV）2组间和组内进行比较,差异均有统计学性意义（P〈0.05）。结论采用依帕司他联合甲钴胺治疗DPN能明显改善患者症状、体征、传导功能,从而达到良好的治疗效果。     

Mitochondrial loss indicates early axonal damage in small fiber neuropathies

Evaluation of nerve fibers in the skin provides a useful tool for the diagnosis of small fiber neuropathies (SFNs). Our aim was to determine whether mitochondria are involved in SFN, indicating early axonal damage. We quantified mitochondrial respiratory chain complex IV (OXPHOS) and axonal (PGP 9.5) fluorescence on skin sections from 32 SFN patients and 14 healthy controls. Also, a group of six patients were recruited before and after 30-day treatment with the mitotoxic antibiotic linezolid. We measured the co-localization of OXPHOS within the intraepidermal and subpapillary dermal axons (PGP-immunoreactive [PGP-ir]). SFN patients with relatively preserved intraepidermal nerve fibers (SFN borderline) showed statistically significant reduction of OXPHOS (50.5 ± 33.9 μm(2) vs. 107.6 ± 81 μm(2) in controls, p < 0.02). A positive correlation was found between both PGP-ir and OXPHOS in controls (Pearson's coefficient r = 0.59, p < 0.001), whereas such correlation was absent in SFN. With respect to baseline measurements, linezolid therapy increased both PGP-ir and OXPHOS, which could be considered an initial compensatory toxic-induced response. This study set out to identify a possible marker of axonal pre-degenerative state in SFN borderline patients.     

Validation of a Brazilian quantitative sensory testing (QST) device for the diagnosis of small fiber neuropathies

Quantitative sensory testing (QST) is defined as the determination of thresholds for sensory perception under controlled stimulus. Our aim was to validate a new QST device for Brazilian sample. In 20 healthy adults, thermoalgesic thresholds were assessed using a QST prototype (Heat Pain Stimulator-1.1.10; Brazil). A 30 × 30 mm(2) thermode with a 1°C/s stimulus change rate were applied. Thresholds of three consecutive stimuli were averaged in two different sessions separated by at least two weeks. Additionally long thermal heat pain stimulus was performed. To evaluate the consistency of our method we also analyzed 11 patients with small fiber neuropathy. Results showed good reproducibility of thermal perception thresholds in normal individuals and plausible abnormal thresholds in patients. We conclude that our QST device is reliable when analyzing the nociceptive pathway in controls and patients.     

糖尿病周围神经病的小纤维损害

目的对糖尿病周围神经病患者进行痛觉传导通路研究,评估其小神经纤维功能。方法对56例有疼痛症状的2型糖尿病患者进行感觉传导速度测定和接触性热痛诱发电位检测;同时进行健康对照组测试。结果糖尿病组感觉传导速度和接触性热痛诱发电位检测与对照组比较,各参数差异均有统计学意义。其中Aδ纤维和C纤维传导速度:糖尿病组分别为(8.6±1.7)m/s和(0.9±0.1)m/s,对照组分别(13.1±2.4)m/s和(1.7±0.3)m/s,差异有统计学意义(t=17.23,21.62,P均<0.05)。糖尿病组中,感觉传导速度异常率与接触性热痛诱发电位异常率比较,差异有统计学意义。结论糖尿病周围神经病中存在小神经纤维的传导异常,提示小神经纤维功能受累。     

Immune-mediated neuropathies in myeloma patients treated with bortezomib

OBJECTIVE: Bortezomib is a new chemotherapeutic drug available for the treatment of lymphoid disorders, including multiple myeloma. Although its primary mechanism of action is proteasome inhibition, other mechanisms can contribute to the therapeutic effects, including modulation of inflammatory cytokines and immune response. One of the main toxic effects of bortezomib is peripheral neuropathy, usually occurring in the form of a painful, sensory axonal neuropathy. The mechanisms of peripheral damage, however, are still unclear. We here report a series of patients treated with bortezomib, who developed a peripheral damage possibly related to immuno-mediated, rather than toxic, mechanisms. METHODS: Five patients who developed a peripheral neuropathy with severe motor involvement under bortezomib treatment underwent CSF, electrophysiological, and spinal cord MRI examinations. RESULTS: Peripheral damage was characterized by: demyelinating or mixed axonal-demyelinating neuropathy, with prominent motor involvement; albumin-cytological dissociation; lumbar root enhancement on MRI in 2/5 patients; favourable outcome in 4/5 patients after immune treatments, either steroids (2 patients) or IVIg (2 patients). CONCLUSIONS: In some instances, the peripheral damage associated with bortezomib may recognize immuno-mediated mechanisms. SIGNIFICANCE: This form of bortezomib-associated neuropathy needs to be recognized as treatable condition, as it may respond to immune therapies. Unexplained worsening of neurological dysfunction despite bortezomib discontinuation, with prominent motor involvement and CSF signs of inflammation, may be the clues to this complication.     

A reappraisal of the presence of small or large fiber neuropathy in patients with erythromelalgia

ObjectiveTo assess the contribution of large and small nerve fiber alteration in erythromelalgia (EM).MethodsThirty-three EM patients were included and underwent clinical evaluation based on EM severity score, DN4, and Utah Early Neuropathy Scale (UENS) score. Neurophysiological evaluation consisted in nerve conduction studies (NCS) for large nerve fibers and specific tests for small nerve fibers: electrochemical skin conductance, cold and warm detection thresholds, and laser evoked potentials. Finally, the evaluation of vascular changes was based on the presence of clinical feature of microvascular disorders and the measurement of the Toe Pressure Index (TPI).ResultsWhile 28 patients (85%) had vascular alteration on TPI or clinical features, 23 patients (70%) had small-fiber neuropathy on neurophysiological tests, and only 10 patients (30%) had large fiber neuropathy on NCS. Regarding clinical scores, there was no difference between groups (presence or absence of large- or small-fiber neuropathy or microvascular disorder) except for a higher UENS score in patients with large fiber neuropathy.ConclusionPeripheral neuropathy, mostly involving small nerve fibers, is almost as common as microvascular changes in EM, but remains inconstant and not related to a specific neuropathic pattern or higher clinical severity.SignificanceThe association of neuropathic and vascular factors is not systematic in EM, this syndrome being characterized by different pathophysiological mechanisms leading to a common clinical phenotype.     

Functional health status of patients with chronic inflammatory neuropathies

The functioning of 12 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and 18 patients with multifocal motor neuropathy (MMN) was evaluated to obtain health profiles and appropriate clinimetric instruments. Assessment was made in a cross-sectional study by means of a performance-based body function test (hand-held dynamometry), two performance-based activity tests (10-m walk test and Berg balance scale), a self-reported activity test (Canadian Occupational Performance Measure), and a self-reported functioning test (sickness impact profile 68). In both patient groups, CIDP and MMN, specific health profiles were manifest. A clear relationship between body function, activities, and functioning was not found. Therefore, to assess a patient with inflammatory neuropathy, it is recommended to assess body function as well as activities and functioning and to select appropriate clinimetric instruments specific for each type of neuropathy.